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Phenobarbital Level 

  • Author: Suzanne Bentley, MD; Chief Editor: Eric B Staros, MD  more...
 
Updated: Jan 03, 2014
 

Reference Range

Phenobarbital is a barbiturate that reduces excitatory synaptic responses by acting on GABAA receptors. It is most commonly used in the treatment of seizures, including tonic-clonic seizures and in status epilepticus. Studies have also shown its efficacy in treating benzodiazepine toxification and perinatal asphyxia.[1, 2]

The therapeutic reference range of phenobarbital varies by age, as follows:

  • Infants and children (< 5 years): 15-30 µg/mL
  • Adults: 15-40 µg/mL

The minimum toxic level is 30 µg/mL.

The toxic concentration/critical laboratory value is 60 µg/mL or more.

The normal terminal elimination half-life also varies by age, as follows:

  • Infants and children (< 5 years): 40-70 hours
  • Adults: 50-140 hours

Phenobarbital’s usual duration of effect exceeds 6-12 hours.

The volume of distribution is 0.5-1 L/kg.

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Interpretation

The phenobarbital level is used to measure the concentration of the drug in a patient’s blood.

The phenobarbital level can be correlated with a patient’s clinical presentation to ascertain the therapeutic phenobarbital level. Of note, other medications, including antihistamines, corticosteroids, oral contraceptives, and other antiepileptics, may alter the serum level of phenobarbital; therefore, it is important to closely monitor patients receiving these medications to closely monitor phenobarbital levels.

Phenobarbital levels must be monitored for the entire administration duration.

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Collection and Panels

Specimen: Whole blood/serum/plasma

Container: Red-top tube (plain, no gel)

Collection method: Routine venipuncture

Draw volume: 1 mL; 0.4 mL is the minimum

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Background

Description

Phenobarbital is a barbiturate that reduces excitatory synaptic responses by acting on GABAA receptors. It is most commonly used in the treatment of seizures, including tonic-clonic seizures and in status epilepticus. Phenobarbital is usually a second- or third-line agent for these indications (after diazepam or phenytoin), as the onset of drug effects are delayed. The onset of effect after intravenous phenobarbital administration is within 5 minutes, and peak effects occur within 30 minutes. The only possible exception to this rule is in the case of drug-induced seizures, particularly with seizures secondary to theophylline ingestion, in which phenobarbital may be administered prior to phenytoin.

Symptoms of phenobarbital toxicity include sedation, ataxia, nystagmus, hyperactivity and irritability (in pediatric patients), and confusion and agitation (in elderly populations). Moreover, sedation can be seen in all patients upon initiation of therapy, but tolerance to this symptom occurs with chronic dosing. Phenobarbital, when combined with other sedative medications, has additive effects on both CNS and respiratory depression.

Indications/Applications

There is no exact relationship between the concentration of phenobarbital in the plasma and its therapeutic effects, however, plasma levels of 10-35 µg/mL are recommended for seizure management. Steady state is usually attained between 2-3 weeks after initiation of drug therapy.

Phenobarbital is metabolized principally in liver by microsomal enzymes, with up to 25% of the phenobarbital dose eliminated by pH-dependent renal excretion. The drug is contraindicated in patients with hepatic dysfunction (as it can increase the half-life) and porphyria. With long-term use, phenobarbital can induce hepatic CYP enzymes—principally CYP2C9. Phenobarbital is 40%-60% bound to plasma proteins and body tissues.

The half-life of phenobarbital increases during pregnancy in part because of volume expansion.

Considerations

Recent studies on phenobarbital level monitoring have examined the effects of age on phenobarbital clearance. A study by Messina et al in 2005 demonstrated that, with age, the rate of phenobarbital clearance decreases. This can be most likely attributed to decreased hepatic drug clearing and decrease in glomerular filtration rate found in the elderly population. As a result, older patients may require a lower dose of phenobarbital to achieve comparable therapeutic effects than younger patients.[3]

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Contributor Information and Disclosures
Author

Suzanne Bentley, MD Assistant Professor, Departments of Emergency Medicine and Medical Education, Elmhurst Hospital, Mount Sinai School of Medicine

Suzanne Bentley, MD is a member of the following medical societies: American College of Emergency Physicians, American Medical Association, American Medical Womens Association, Society for Academic Emergency Medicine, Emergency Medicine Residents' Association

Disclosure: Nothing to disclose.

Chief Editor

Eric B Staros, MD Associate Professor of Pathology, St Louis University School of Medicine; Director of Clinical Laboratories, Director of Cytopathology, Department of Pathology, St Louis University Hospital

Eric B Staros, MD is a member of the following medical societies: American Medical Association, American Society for Clinical Pathology, College of American Pathologists, Association for Molecular Pathology

Disclosure: Nothing to disclose.

Acknowledgements

Christie Lech, MD Resident Physician, Department of Emergency Medicine, Mount Sinai School of Medicine of New York University

Christie Lech, MD, is a member of the following medical societies: American College of Emergency Physicians, Emergency Medicine Residents Association, and Society for Academic Emergency Medicine

Disclosure: Nothing to disclose.

References
  1. Kawasaki SS, Jacapraro JS, Rastegar DA. Safety and effectiveness of a fixed-dose phenobarbital protocol for inpatient benzodiazepine detoxification. J Subst Abuse Treat. 2012 Oct. 43(3):331-4. [Medline].

  2. Avasiloaiei A, Dimitriu C, Moscalu M, Paduraru L, Stamatin M. High-dose phenobarbital or erythropoietin for the treatment of perinatal asphyxia in term newborns. Pediatr Int. 2013 Oct. 55(5):589-93. [Medline].

  3. Messina S, Battino D, Croci D, Mamoli D, Ratti S, Perucca E. Phenobarbital Pharmacokinetics in Old Age: A Case-Matched Evaluation Based on Therapeutic Drug Monitoring Data. Epilepsia. 2005. 16(3):372-377.

  4. Brunton LL, Chabner BA, Knollmann BC. Goodman & Gilman's The Pharmacological Basis of Therapeutics, 12e. The McGraw-Hill Companies, Inc; 2011.

  5. Gomella LG, Haist SA. Clinician's Pocket Reference, 11e. The McGraw-Hill Companies, Inc.; 2007.

  6. Olsen K. Poisoning and Drug Overdose, 5e. The McGraw-Hill Companies, Inc.; 2007.

  7. Warner A, Privitera M, Bates D. Standards of Laboratory Practice: Antiepileptic Drug Monitoring. Clinical Chemistry. 1998. 44(5):1085-1095.

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